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Clinical Cardiology Journal

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Christine Pacheco*
 
Cardiovascular Division, University of Florida, Gainesville, Florida, USA, Email: [email protected]
 
*Correspondence: Christine Pacheco, Cardiovascular Division, University of Florida, Gainesville, Florida, USA, Email: [email protected]

Received Date: Sep 07, 2021 / Accepted Date: Sep 21, 2021 / Published Date: Sep 28, 2021

Citation: Pacheco C. An overview on coronary microvascular dysfunction (CMVD). Clin Cardiol J 2021;5(5):1.

This open-access article is distributed under the terms of the Creative Commons Attribution Non-Commercial License (CC BY-NC) (http://creativecommons.org/licenses/by-nc/4.0/), which permits reuse, distribution and reproduction of the article, provided that the original work is properly cited and the reuse is restricted to noncommercial purposes. For commercial reuse, contact [email protected]

Commentary

Patients with Coronary Microvascular Dysfunction (CMVD) are a common occurrence, and despite the fair prognosis, many of them have a poor quality of life due to angina symptoms that limit their daily activities. The most common clinical presentation pictures, such as stable and unstable microvascular angina, are summarized in this article. The main risk factors are discussed, followed by the most recent information on the topic, including pathogenic hypotheses, diagnostics, and treatment options. Microvascular abnormalities that aren’t fully understood, such as slow flow and no reflow are explored, as well as prognosis and the disease’s influence on quality of life. Angina without Coronary Artery Disease (CAD) is associated with significant morbidity and is found in 10% to 30% of individuals who undergo angiography. In 50 percent to 65 percent of these patients, Coronary Microvascular Dysfunction (CMD) is evident. The best treatment for this group is unknown.

In the absence of CAD, we conducted a systematic review to assess therapeutic options for objectively diagnosed CMD. We included studies using positron emission tomography, cardiac magnetic resonance imaging, dilution methods, or intracoronary Doppler in human subjects with angina and a coronary flow reserve or myocardial perfusion reserve of 2.5 in the absence of coronary artery stenosis of 50% or structural heart disease. Only eight papers satisfied the stringent standards for inclusion. Different treatments, outcomes, and definitions of CMD were used in the publications. With an average of 11 patients per investigation, the small sample sizes substantially restrict the power of this research studies looking at the effects of sildenafil, quinapril, oestrogen and transcutaneous electrical nerve stimulation all showed positive results.

L-arginine, doxazosin, pravastatin, and diltiazem showed no benefit. Our systematic review found that there is little evidence to support CMD therapies. We evaluate material that meets stringent inclusion requirements and examine previously published data that is related but not included. We also go over the next stages in closing this research gap, which include a consistent definition of CMD, routine CMD assessment in studies of chest pain without obstructive CAD, and specific therapy assessment in the population with confirmed CMD. At this moment, we don’t know enough about the relevance, processes, and consequences of coronary microvascular dysfunction linked with diabetes mellitus. Endothelial dysfunction induced by diabetes in various arterial beds is well known for contributing to a wide range of problems and having negative effects on microcirculatory control. The coronary microcirculation is controlled by a series of interrelated physiological processes that aim to adapt local blood flow to myocardial metabolic needs. This network’s dysregulation could have varied degrees of pathogenic repercussions.

From a preclinical and clinical standpoint, this review highlights the most relevant results addressing coronary microvascular dysfunction in diabetes. Left Ventricular Hypertrophy (LVH) is a condition in which the left myocardial mass grows due to an increase in cardiomyocyte size. LVH can be a physiological response to physical activity or a pathological condition that is either primary (i.e. genetic) or secondary (i.e. caused by LV ovulation). There is evidence of coronary microvascular dysfunction in both primary and secondary LVH patients (CMD). Capillary rarefaction and unfavourable remodelling of intramural coronary arterioles due to medial wall thickening with an elevated wall/lumen ratio are the main causes of the latter.

The widespread scope of this remodelling, which affects coronary micro vessels across the left ventricle, is a key characteristic of these phenomena. Heart Failure with Preserved Ejection Fraction (HFpEF) and Heart Failure with Reduced Ejection Fraction (HFrEF) can occur in patients with LVH caused by arterial hypertension (HFrEF). These patients can develop HFrEF by a ‘direct pathway’ with or without an interval myocardial infarction. Patients with HFpEF, on the other hand, can proceed to HFrEF with or without interval myocardial infarction. Patients with hypertrophic cardiomyopathy, the most common hereditary cardiomyopathy with a pattern marked by large LVH, can experience a similar progression to LV dysfunction and both HFpEF and HFrEF. We will examine both experimental and clinical findings that explain the mechanisms behind CMD in LVH, as well as data linking CMD to HFpEF and HFrEF, in this review paper. Angina has long been assumed to be caused by a variety of factors. When coronary angiography is performed on a large number of individuals with angina, it is discovered that they do not have obstructive CAD.

A considerable number of these patients exhibit Coronary Microvascular Dysfunction (CMD), which is defined as an increased sensitivity to vasoconstrictor stimuli and a reduced capacity for microvascular vasodilation. In the last two decades, the coronary microvasculature has been investigated more thoroughly thanks to the development of non-invasive and invasive procedures. In addition to classic atherosclerotic disease and vasospastic illness, CMD has been recognised as a cause of cardiac ischemia. CMD can arise on its own or in conjunction with obstructive CAD. CMD and macrovascular CAD have many risk factors in common. The attenuation of coronary blood flow in response to vasodilatory drugs is used to diagnose the condition. Traditional intracoronary vaso-reactivity testing has not yet been totally superseded by imaging modalities such as cardiovascular magnetic resonance, positron emission tomography, and transthoracic Doppler echocardiography. CMD treatment begins with a change in lifestyle and the management of risk factors. Traditional antianginal, anti-atherosclerotic drugs, as well as some novel therapies, may be useful; nevertheless, clinical trials are required to determine the efficacy of pharmacologic and nonpharmacologic therapy approaches. Furthermore, longer-term studies are required to assess the prognostic benefits of these medicines. The epidemiology, prognosis, pathophysiology, diagnosis, risk factors, and current treatments for CMD are all discussed.

 
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